The defeat of the block (IV) nerve (n. Trochlearis)

Symptoms of affection of the nerve block

The acute onset of vertical diplopia in the absence of ptosis in combination with the characteristic position of the head is typical for affection of the nerve block. Manifestations of nuclear, bundle and peripheral lesions of the nerve block are clinically identical except for the fact that nuclear damage causes weakness of the contralateral superior oblique muscle. The lesion of the left block nerve is illustrated.

• It is limited to lowering the eye on the left side due to weakness of the upper oblique muscle.
• Excl. Excision.
• Vertical torsion diplopia, increasing when looking down.
• Hyperdeviation of the left eye ("left over right") in the primary position, when the intact right eye fixes, due to the weakness of the left upper oblique muscle.
• Hypertrophy of the left eye is enhanced when viewed to the right due to the hyperactivity of the left lower oblique muscle and is minimal or absent when viewed to the left.

The forced position of the head is taken to eliminate diplopia.

• With the rotation of the eye (softens the exclusion) there is a contralateral inclination of the head.
• With the inability to lower the eye when casting, the face is turned to the right, and the chin is lowered.

The left eye can not be looked down and to the right or rotated by it. This compensates for the movement of the head.

Two-sided lesions of the nerve block are characterized by:

• Hypertrophy of the right eye when viewed from the left, left - when viewed to the right.
• Cyclodeaviation is more than 10 for a double test with a Maddox stick.
• V-pattern of the zosotropy.
• Two-sided positive test Bielschowsky.

Causes of isolated lesion of the nerve block

1. Congenital lesions are frequent, but the symptoms may not develop until adulthood. Studying old photographs for the presence of an abnormal position of the head can help in the same way as the increased fuzzy range in the vertical prism.
2. Trauma often leads to bilateral lesions of the IV pair of cranial nerves. Long and thin nerves are vulnerable to the physical effect of the tentorial margin in the upper cerebral sail, where they cross.
3. Vascular lesions are frequent, and aneurysms and tumors are rare.

Patients with damage to the nerve block complain of vertical dilation, which is most pronounced when looking down and in the opposite direction. This picture is caused by the one-sided paralysis of the upper oblique muscle of the eye (m. Obliquus superior), turning the eyeball outwards and downwards. Patients with this paralysis tend to tilt their head in the opposite direction to the paretic muscle to reduce the feeling of double vision (less often the head is tilted toward the paralysis, which presumably allows the patient to more clearly isolate the visual image on the retina of one eye and ignore it on the other). It must be remembered that paralysis of the upper oblique muscle may be accompanied by signs of hyperactivity and even contracture of the lower oblique muscle. The defeat of the nerve block is less often recognized than the damage of the III or VI nerves.

Paralysis of the nerve block can be one-sided and two-sided.

Topical diagnosis of lesion of the nerve block is possible on the following four levels:

• I. The level of the nucleus or root of the nerve block (or both) in the brain stem.
• P. Nerve level in the subarachnoid space.
• III. The level of the nerve block in the cavernous sinus.
• IV. Nerve level in orbit.

I. Damage to the nerve block at the level of its nucleus or root (or both) in the brain stem. This paralysis of the upper oblique muscle contralateral damage.

Depending on what adjacent structures of the brain stem are involved in the pathological process, the following clinical picture can be observed:

Involving only one nucleus or root of the IV nerve (rarely) is accompanied only by a picture of isolated lesion of the nerve block.

The defeat of the prefectural area leads to vertical paralysis of the gaze (dorsal midbrain syndrome). The defeat of the upper leg of the cerebellum is accompanied by dissymmetry on the side of the lesion.

The involvement of descending sympathetic fibers is manifested by Horner's syndrome on the side of the lesion. The involvement of the posterior (medial) longitudinal fascicle is manifested by ipsilateral paresis of the muscle, which leads the eyeball with nystagmus in the contralateral eyeball when it is withdrawn.

The defeat of the upper dichotomy leads to a contralateral syndrome of the so-called relative afferent pupillary defect (the pupil of Marcus-Gunn or the asymmetry of the pupils' reaction to light, a normal direct reaction of both pupils to light is observed, with a rapid alternation of illumination of one and the other eye, when moving the light source from the healthy side to the affected one) without visual disturbances.

The defeat of the anterior cerebral sail is accompanied by a bilateral defeat of the nerve block.

II. Damage to the nerve block in the subarachnoid space leads to ipsilateral paralysis of the superior oblique muscle, if the mesencephalus is not compressed.

The defeat of only one IV nerve is accompanied only by a picture of isolated lesion of the nerve block.

The defeat of the upper leg of the cerebellum is accompanied by ipsilateral dysmetry.

The defeat of the brain stem is accompanied by contralateral hemiparesis.

III. The defeat of the nerve block in the cavernous sinus and (or) the upper orbital fissure

The defeat of only one IV nerve is accompanied only by a picture of isolated lesion of the nerve block (rarely). Involvement of III, VI cranial nerves and sympathetic fibers leads to ophthalmoplegia; the pupil can be small, wide, or preserved; Ptosis is observed. Involving the V cranial nerve (the first branch) is accompanied by facial or retroorbital pain, a violation of sensitivity in zone I of the trigeminal nerve branch. The increase in venous pressure will be manifested by proptosis (exophthalmos) and chemosis.

IV. Block nerve damage in the eye socket

Damage to the nerve block, the upper oblique muscle or its tendon is manifested by the paralysis of the upper oblique muscle.

Mechanical limitation of the tendon of the upper oblique muscle leads to the syndrome of Brown (strongrown): a form of strabismus, in which fibrosis and shortening of the upper oblique muscle of the eye is observed, which leads to a characteristic restriction of the movements of the eyeball.

Involvement of other motor nerves of the eyeball or external muscles of the eye leads to ophthalmoplegia, ptosis, and restriction of movements of the eyeball. The involvement of the optic nerve is manifested by a decreased vision, edema or atrophy of the optic disc. The mass effect is manifested by exophthalmos (sometimes enophthalmos), chemosis, eyelid edema.

The main causes of unilateral or bilateral lesion of the nerve block: trauma (including neurosurgical and spinal anesthesia), aplasia of the nerve nucleus, mesencephalic ischemic or hemorrhagic stroke, tumor, arteriovenous malformation, demyelination, subdural hematoma with compression of the brainstem, ischemic neuropathy of the IV nerve with sugar diabetes or other vasculopathies, Guillain-Barre syndrome (other cranial nerves are involved), ophthalmic herpes zoster (rare), neonatal hypoxia, encephalitis, complicated cardiac surgery, volumetric and infiltrative processes in orbit. Rare reasons for isolated paralysis of the upper oblique muscle of the eye is myasthenia gravis or distyroidoid orbitopathy.

Most lesions of the nucleus of the nerve block are accompanied by the involvement of nearby structures. Quite often ipsalateral cerebellar signs are observed. Involvement of the nucleus of the nerve block or its root leads to contralateral paresis of the upper oblique muscle of the eye. One-sided damage to the nucleus or root of the nerve before its cross in the anterior cerebral sail with the involvement of sympathetic fibers can cause ipsilateral Gorner's syndrome and contralateral paresis of the upper oblique muscle of the eye. One-sided mesencephalic damage to the nucleus of the nerve block (or its fibers before the cross) and the medial longitudinal bundle can cause ipsilateral interocular ophthalmoplegia and contralateral paralysis of the upper oblique muscle of the eye. A lesion involving the upper dioecium and the underlying nucleus of the nerve block or its spine can cause a contralateral relative afferent pupillary defect without visual disturbances and a contralateral paresis of the upper oblique muscle of the eye. The bilateral paresis of the superior oblique muscle with symptoms of involvement of the spinotalamic tract on one side is described with a small spontaneous hemorrhage in the area of the mesencephalon cover.

Isolated myoclymic obliquus superior usually has a benign course (but is described as a sign of affecting the middle brain) and is not accompanied by symptoms of paralysis of this muscle.

[1], [2]